• BMB Reports
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• v.37 no.4
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• pp.402-407
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• 2004

A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCP10L in human hepatocarcinomas.

• Molecules and Cells
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• v.26 no.4
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• pp.350-355
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• 2008

Chk2 is a well characterized protein kinase with key roles in the DNA damage response. Chk2 is activated by phosphorylation following DNA damage, and relays that signal to various substrate proteins to induce cell cycle arrest, DNA repair, and apoptosis. In order to identify novel components of the Chk2 signaling pathway in Drosophila, we screened 2,240 EP misexpression lines for dominant modifiers of an adult rough eye phenotype caused by Chk2 overexpression in postmitotic cells of the eye imaginal disc. The rough eye phenotype was suppressed by mutation of the ATM kinase, a well-described activator of Chk2. Twenty-five EP modifiers were identified (three enhancers and 22 suppressors), none of which correspond to previously known components of Chk2 signaling. Three EPs caused defects in G2 arrest after irradiation with incomplete penetrance when homozygous, and are likely directly involved in the response to DNA damage. Possible roles for these modifiers in the DNA damage response and Chk2 signaling are discussed.

• Molecules and Cells
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• v.37 no.2
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• pp.187-187
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• 2014

• Proceedings of the Zoological Society Korea Conference
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• 2003.08a
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• pp.211.3-211
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• 2003

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1996.04a
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• pp.24-24
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• 1996

No Abstract, See Full Text

• The Journal of Korean Society of Virology
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• v.30 no.3
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• pp.161-170
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• 2000

Continuous efforts are being made to find effective therapeutic agents against HIV-1, the causative agents of AIDS. In this study, we developed a cell-based assay system employing a trans-complementation for production of recombinant viruses which are capable of undergoing one round of replication in CD4+ T cells. This assay system was tested for ability to screen the agents that act at late stage of HIV-1 life cycle. The effect of a protease inhibitor on the trans-complementation assay was assessed. Recombinant HIV-1 viruses were prepared from a trans-complementation in the presence of various concentrations of protease inhibitor. Inhibition of single round infection of these recombinant viruses by protease inhibitor was observed to be a dose-dependent manner. Inhibitory effects of a protease inhibitor on HIV-1 Gag polyprotein processing by HIV-1 protease was detected at concentrations of the protease inhibitor compatible with inhibition of virus infection, confirming that the corresponding step was involved in the inhibitory mechanism of this compound. Together, these results provide evidence that a cell-based assay system established in this study can be used to screen the agents that target the late stage of HIV-1 life cycle.

• Proceedings of the Zoological Society Korea Conference
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• 1996.10a
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• pp.246.1-246
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• 1996

No Abstract, See Full Text

• Journal of Interdisciplinary Genomics
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• v.4 no.1
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• pp.15-18
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• 2022

Hemophilia A is a rare X-linked congenital deficiency of clotting factor VIII (FVIII) that is traditionally diagnosed by measuring FVIII activity. Various mutations of the FVIII gene have been reported and they influence on the FVIII protein structure. A deficiency of or reduction in FVIII protein manifests as spontaneous or induced bleeding depending on the disease severity. Mutations of the FVIII gene provide important information on the severity of disease and inhibitor development. FVIII mutations also affect the discrepant activities found using different FVIII assays. FVIII activity is affected differently depending on the mutation site. Long-range PCR is commonly used to detect intron 22 inversion, the most common mutation in severe hemophilia. However, point mutations are also common in patients with hemophilia, and direct Sanger sequencing and copy number variant analysis are being used to screen for full mutations in the FVIII gene. Advances in molecular genetic methods, such as next-generation sequencing, may enable accurate analysis of mutations in the factor VIII gene, which may be useful in the diagnosis of mild to moderate hemophilia. Genetic analysis is also useful in diagnosing carriers and managing bleeding control. This review discusses the current knowledge about mutations in hemophilia and focuses on the clinical aspects associated with these mutations and the importance of genetic analysis.

• Journal of Preventive Medicine and Public Health
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• v.40 no.2
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• pp.102-107
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• 2007

Human Genome Project (HGP) could unveil the secrets of human being by a long script of genetic codes, which enabled us to get access to mine the cause of diseases more efficiently. Two wheels for HGP, bioinformatics and high throughput technology are essential techniques for the genomic medicine. While microarray platforms are still evolving, we can screen more than 500,000 genotypes at once. Even we can sequence the whole genome of an organism within a day. Because the future medicne will focus on the genetic susceptibility of individuals, we need to find genetic variations of each person by efficient genotyping methods.

• Animal cells and systems
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• v.1 no.2
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• pp.355-361
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• 1997

We have screened available chromosomal deficiencies on the X chromosome for genetic loci whose zygotic expression is required for body-wall muscle development during embryogenesis in Caenorhabditis elegans. Previously, it had been reported that no sign of muscle development was detected in nullo-X embryos arrested at an early stage of embryogenesis. Based on this observation, it has been suggested that genetic loci exist on the X chromosome whose zygotic expression is essential for body-wall muscle formation. In order to identify such myogenic loci, 9 chromosomal deficiencies covering approximately 45% of the X chromosome have been tested. Homozygous embryos from these deficiency strains were collected and terminal phenotypes of arrested embryos were observed by Nomarski microscopy. As a secondary assay, monoclonal antibodies against two myosin heavy chain (MHC) isoforms, the products of the myo-3 and unc-54 genes, were used to detect body-wall muscle differentiation. All the homozygous deficiency embryos were positively stained with both MHC antibodies and muscle twitching movement was observed in most cases. Combined with previously analyzed deficiencies, our deficiency screen has covered approximately 70% of the X chromosome. We conclude that the regions covered by the available deficiencies on the X chromosome do not include any myogenic locus required for body-wall muscle formation. Alternatively, the possibility that nullo-X embryo may not form body-wall muscle due to a general failure to differentiate during embryogenesis remains to be tested.